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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
1
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pubmed:dateCreated |
2008-12-23
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pubmed:abstractText |
Trophoblast expression of immunomodulatory proteins in the human placenta is among the mechanisms that are critical for ensuring lymphocyte tolerance to the semi-allogeneic fetus. High levels of B7-H1 on trophoblast cells together with the known role of this protein in establishment of peripheral tolerance suggest that B7-H1 mediates immunological protection of the placenta during gestation. In this study, we investigated the molecular mechanisms of regulation of B7-H1 in trophoblast cells by epidermal growth factor (EGF), a key regulator of trophoblast cell differentiation. EGF increased B7-H1 protein levels within 24 h and mRNA levels within 4h of the initiation of treatment; by 24 h B7-H1 mRNA levels were similar between control and EGF-treated cells. Analysis of two different potential promoter regions revealed strong promoter activity in response to IFN-gamma. In contrast, no promoter activity could be induced by EGF, suggesting that this cytokine regulates B7-H1 expression post-transcriptionally in trophoblast cells. EGF-induced B7-H1 protein expression was completely blocked in the presence of inhibitors of the PI3Kinase/Akt/mTOR pathway, a pathway known to regulate gene expression at the translational level. Finally, analysis of monosomal and polysomal mRNA fractions of untreated and EGF-treated term trophoblast cells revealed that EGF induces a shift towards the translatable fractions and away from the untranslated fractions. These results highlight a novel mechanism for regulation of B7 family proteins in the placenta.
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pubmed:grant |
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pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/19010538-10485649,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19010538-10579998,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19010538-10581077,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19010538-11015443,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19010538-11135580,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19010538-11209085,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19010538-11224527,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19010538-11978065,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19010538-12089343,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19010538-12091876,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19010538-12411397,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19010538-12606489,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19010538-15030776,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19010538-15235105,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19010538-15249675,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19010538-15292274,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19010538-15771580,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19010538-15993704,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19010538-16027236,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19010538-16236361,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19010538-16251499,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19010538-16251747,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19010538-16382236,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19010538-16413538,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19010538-16921384,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19010538-16972895,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19010538-17041626,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19010538-17159987,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19010538-17376031,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19010538-18223165,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19010538-9290154
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD,
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD274,
http://linkedlifedata.com/resource/pubmed/chemical/CD274 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Enzyme Inhibitors,
http://linkedlifedata.com/resource/pubmed/chemical/Epidermal Growth Factor,
http://linkedlifedata.com/resource/pubmed/chemical/Interferon-gamma,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger
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pubmed:status |
MEDLINE
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pubmed:month |
Jan
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pubmed:issn |
0143-4004
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:volume |
30
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
48-55
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pubmed:dateRevised |
2011-11-17
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pubmed:meshHeading |
pubmed-meshheading:19010538-Adult,
pubmed-meshheading:19010538-Antigens, CD,
pubmed-meshheading:19010538-Antigens, CD274,
pubmed-meshheading:19010538-Cell Differentiation,
pubmed-meshheading:19010538-Cell Fusion,
pubmed-meshheading:19010538-Cell Separation,
pubmed-meshheading:19010538-Cells, Cultured,
pubmed-meshheading:19010538-Chorionic Villi,
pubmed-meshheading:19010538-Enzyme Inhibitors,
pubmed-meshheading:19010538-Epidermal Growth Factor,
pubmed-meshheading:19010538-Female,
pubmed-meshheading:19010538-Gene Expression,
pubmed-meshheading:19010538-Humans,
pubmed-meshheading:19010538-Interferon-gamma,
pubmed-meshheading:19010538-Pregnancy,
pubmed-meshheading:19010538-Protein Processing, Post-Translational,
pubmed-meshheading:19010538-RNA, Messenger,
pubmed-meshheading:19010538-Trophoblasts,
pubmed-meshheading:19010538-Young Adult
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pubmed:year |
2009
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pubmed:articleTitle |
Differentiation-induced post-transcriptional control of B7-H1 in human trophoblast cells.
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pubmed:affiliation |
Department of Anatomy and Cell Biology, University of Kansas Medical Center, 3901 Rainbow Boulevard, Kansas City, KS 66160, USA.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't,
Research Support, N.I.H., Extramural
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